The hemodynamic destruction of intravascular cancer cells in relation to myocardial metastasis.

Publisher Website
Google Scholar
Abstract
A variety of observations in humans and experimental animals indicate that large numbers of circulating cancer cells are killed in the microvasculature. It is suggested that this occurs when friction or adhesion between individual cancer cells and capillary walls results in an increase of tension in the cancer cell peripheries above a critical level because of (blood) pressure differentials between their free ends. Hemodynamic and anatomic data relating to the myocardial circulation and deformability measurements on four types of rat cancer cells have been reported previously by others. Novel calculations based on these data suggest that the increased tension at the peripheries of cancer cells passing through the myocardial capillaries will exceed the critical levels for rupture. Analysis of autopsy data for solid tumors reveals a low (less than 3%) incidence of myocardial metastases in the absence of lung metastases and a higher (15%) incidence in their presence. One explanation for these observations is that, in the absence of lung metastases, relatively few of the cancer cells enter the coronary arteries from primary tumors with systemic venous drainage because many are retained or destroyed in transit through the pulmonary vasculature, and most of those delivered to the myocardium then suffer hemodynamic destruction. In the presence of pulmonary metastases, large numbers of viable cancer cells are liberated directly into the pulmonary venules and subsequently are delivered to the myocardium without prior exposure to the arterial side of the microcirculation. The combined effects of increased delivery and the protective effects of arrested cells on those preceding them in files along the capillaries account for the higher incidence of myocardial metastases. It is proposed that hemodynamic destruction of circulating cancer cells may be an important underlying cause of metastatic inefficiency, together with other cytocidal mechanisms.